Aim: To investigate the androgen receptor (AR) isoform expressions in human prostatic cancer tissue and LNCaPcell line. Methods: With high resolution isoelectric focusing (IEF) method we demonstrated the different exp...Aim: To investigate the androgen receptor (AR) isoform expressions in human prostatic cancer tissue and LNCaPcell line. Methods: With high resolution isoelectric focusing (IEF) method we demonstrated the different expres-sions of AR isoforms in human prostatic cancer tissues and LNCaP cell line. Results; Data were obtained from threeprostatic cancer specimens and the LNCaP cell line. Three types of AR isoforms were detected with pI values at 6.5,6.0, and 5.3. For the 3 prostatic cancer specimens, 1 sample showed all the three types of AR isoforms, the secondspecimen expressed at 6.5 and 6.0, and the third failed to show any type of isoforms. The LNCaP cell line expressedall the three AR isoforms. Binding of ~3H-dihydrotestosterone (~3H-DHT) to these three isoforms was inhibited by the ad-dition of 100-fold excess of DHT or testosterone, while not by progesterone, oestradiol and diethylstilboestrol. Conclu-sion : The expression of AR isoforms is different in different prostate cancer tissues, which may be related to the dif-ference in the effect of anti-androgen therapy in different patients. (Asian J Androl 2001 Sep; 3: 223 - 225)展开更多
Objective:To study the expression of TRPC6 among prostate cancer cells,establish high expression cell lines of TRPC6,and to provide potential cell mode for prostate cancer oncogenesis and development.Methods:Occurrenc...Objective:To study the expression of TRPC6 among prostate cancer cells,establish high expression cell lines of TRPC6,and to provide potential cell mode for prostate cancer oncogenesis and development.Methods:Occurrence and development of prostate cancer cells,PC3,PC—3m DU145,22 rvl,LNCaP and normal prostate epithelial cells in the PrEC TRPC6 expression level were detected by QPCR method.Calcium phosphate transfection method was used to package retrovirus pLEGFP-Nl-TRPC6 and pLEGFP-Nl-vector and infect the prostate cancer cells,a stable high expression of TRPC6 prostate cancer cells.Sable cell lines of TRPC6,matrix metalloproteinase(MMP)2,MMP9 expression was detected by QPCR and Western blot.Change of cell invasion ability was detected by Transwell.Results:The expression level of prostate cancer cells TRPC6 were higher than control group PrEC cells.Among TPRC6 the expression of cell line PC 3 transfer potential wre the lowest,and high transfer cell tone PC-3M express was the highest.Real-time fluorescent quantitative PCR and western blot results showed that after filter,the seventh generation of cell TRPC6 protein and mRNA expression levels were higher than the control group obviously.Transwell experimental results showed that the overexpression of TRPC6could promote the invasion ability of PC.3 prostate cancer cells.Conclusions:TRPC6 expressed in prostate cancer cells is in disorder,and its action may be associated with the invasion and metastasis of prostate cancer cells;successful establishment of stable high expression of TRPC6prostate cancer cells primarily confirm the invasion-trigger ability of TRPC6 on prostate cancer,and lay down the foundation for exploring the TRPC6's role in the occurrence and development of prostate cancer展开更多
Aim： To evaluate the antiproliferative activity of contragestazol （DL111-IT） on the human prostate cancer cell line PC3 in vitro and in vivo and to elucidate its potential molecular mechanisms. Methods： The cell k...Aim： To evaluate the antiproliferative activity of contragestazol （DL111-IT） on the human prostate cancer cell line PC3 in vitro and in vivo and to elucidate its potential molecular mechanisms. Methods： The cell killing ability of DL111-IT was measured by the 3-（4,5-dimethylthia-zol,2-yl）-2,5-diphenyltetrazolium bromide （MTT） reagent assay method and the tumor xenograft model. The cell cycle was analyzed by flow cytometry and protein expression, including retinoblastoma （pRb）, cyclin-dependent kinase 4 （CDK4） and cyclin D 1, was detected by Western blotting. Results： DL111-IT exhibited high efficiency on cell growth inhibition of the human androgen-independent prostate cancer cell line PC3. The drug concentration that yielded 50 % cell inhibition （IC50 value） was 9.9 mg/mL. In the PC3 tumor xenograft study, DL111-IT （1.25 mg/kg-20.0 mg/kg） given once a day for 10 days significantly inhibited tumor growth, with the inhibition rate ranging from 21% to 50 %. Flow cytometric analysis indicated that DL111-IT could cause GI arrest in the PC3 cell line, but not apoptosis. DL111-IT enhanced pRb expression and down-regulated CDK4 and cyclin D 1 expression, suggesting that cell cycle regulation might contribute to the anticancer property of DL 111- IT. Conclusion： DL111-1T inhibits the proliferation of human androgen-independent prostate cancer cell line PC3 in vitro and in vivo by a cell cycle regulation pathway.展开更多
文摘Aim: To investigate the androgen receptor (AR) isoform expressions in human prostatic cancer tissue and LNCaPcell line. Methods: With high resolution isoelectric focusing (IEF) method we demonstrated the different expres-sions of AR isoforms in human prostatic cancer tissues and LNCaP cell line. Results; Data were obtained from threeprostatic cancer specimens and the LNCaP cell line. Three types of AR isoforms were detected with pI values at 6.5,6.0, and 5.3. For the 3 prostatic cancer specimens, 1 sample showed all the three types of AR isoforms, the secondspecimen expressed at 6.5 and 6.0, and the third failed to show any type of isoforms. The LNCaP cell line expressedall the three AR isoforms. Binding of ~3H-dihydrotestosterone (~3H-DHT) to these three isoforms was inhibited by the ad-dition of 100-fold excess of DHT or testosterone, while not by progesterone, oestradiol and diethylstilboestrol. Conclu-sion : The expression of AR isoforms is different in different prostate cancer tissues, which may be related to the dif-ference in the effect of anti-androgen therapy in different patients. (Asian J Androl 2001 Sep; 3: 223 - 225)
基金supported by Sichuan Province Department of Health(Grant Project:130188)
文摘Objective:To study the expression of TRPC6 among prostate cancer cells,establish high expression cell lines of TRPC6,and to provide potential cell mode for prostate cancer oncogenesis and development.Methods:Occurrence and development of prostate cancer cells,PC3,PC—3m DU145,22 rvl,LNCaP and normal prostate epithelial cells in the PrEC TRPC6 expression level were detected by QPCR method.Calcium phosphate transfection method was used to package retrovirus pLEGFP-Nl-TRPC6 and pLEGFP-Nl-vector and infect the prostate cancer cells,a stable high expression of TRPC6 prostate cancer cells.Sable cell lines of TRPC6,matrix metalloproteinase(MMP)2,MMP9 expression was detected by QPCR and Western blot.Change of cell invasion ability was detected by Transwell.Results:The expression level of prostate cancer cells TRPC6 were higher than control group PrEC cells.Among TPRC6 the expression of cell line PC 3 transfer potential wre the lowest,and high transfer cell tone PC-3M express was the highest.Real-time fluorescent quantitative PCR and western blot results showed that after filter,the seventh generation of cell TRPC6 protein and mRNA expression levels were higher than the control group obviously.Transwell experimental results showed that the overexpression of TRPC6could promote the invasion ability of PC.3 prostate cancer cells.Conclusions:TRPC6 expressed in prostate cancer cells is in disorder,and its action may be associated with the invasion and metastasis of prostate cancer cells;successful establishment of stable high expression of TRPC6prostate cancer cells primarily confirm the invasion-trigger ability of TRPC6 on prostate cancer,and lay down the foundation for exploring the TRPC6's role in the occurrence and development of prostate cancer
基金This study received financial support from the National Natural Science Foundation of China(No.30000209).
文摘Aim： To evaluate the antiproliferative activity of contragestazol （DL111-IT） on the human prostate cancer cell line PC3 in vitro and in vivo and to elucidate its potential molecular mechanisms. Methods： The cell killing ability of DL111-IT was measured by the 3-（4,5-dimethylthia-zol,2-yl）-2,5-diphenyltetrazolium bromide （MTT） reagent assay method and the tumor xenograft model. The cell cycle was analyzed by flow cytometry and protein expression, including retinoblastoma （pRb）, cyclin-dependent kinase 4 （CDK4） and cyclin D 1, was detected by Western blotting. Results： DL111-IT exhibited high efficiency on cell growth inhibition of the human androgen-independent prostate cancer cell line PC3. The drug concentration that yielded 50 % cell inhibition （IC50 value） was 9.9 mg/mL. In the PC3 tumor xenograft study, DL111-IT （1.25 mg/kg-20.0 mg/kg） given once a day for 10 days significantly inhibited tumor growth, with the inhibition rate ranging from 21% to 50 %. Flow cytometric analysis indicated that DL111-IT could cause GI arrest in the PC3 cell line, but not apoptosis. DL111-IT enhanced pRb expression and down-regulated CDK4 and cyclin D 1 expression, suggesting that cell cycle regulation might contribute to the anticancer property of DL 111- IT. Conclusion： DL111-1T inhibits the proliferation of human androgen-independent prostate cancer cell line PC3 in vitro and in vivo by a cell cycle regulation pathway.
